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  • 1985-1989  (2)
  • Human medullary thyroid carcinoma  (1)
  • Procollagen-III peptide  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 65 (1987), S. 174-178 
    ISSN: 1432-1440
    Keywords: Procollagen-III peptide ; Paget's disease of the bone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A commercially available radioimmunoassay kit was used to determine aminoterminal procollagen-III peptide (pNcoll III) serum levels in patients with Paget's disease of the bone and control subjects. In patients with Paget's disease pNcoll III concentrations were significantly elevated. They decreased to varying degrees under chronic therapy with human and salmon calcitonin, disodium ethane 1-hydroxy 1,1 diphosphonate (EHDP), or a combination therapy of EHDP and human calcitonin. The results were compared with the effect on traditional biochemical markers of disease activity: serum alkaline phosphatase and urinary hydroxyproline excretion, both of which reacted more acutely to the various therapies than pNcoll III, although pretreatment correlations were close. The most probable source of pNcoll III is not the Pagetic bone per se, but the vascular, fibrous connective tissue replacing normal bone marrow.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Voltage dependent calcium channels ; Calcitoninsecretion ; Human medullary thyroid carcinoma ; BAY K 8644-nifedipine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Extracellular calcium concentration is an important regulator of calcitonin secretion. We used primary cell cultures of human medullary thyroid carcinoma to study the role of voltage dependent calcium channels for stimulus secretion coupling. Increasing extracellular calcium concentration (1.6–5.0 mM) in the medium caused a dose dependent release of calcitonin. The calcium channel activator BAY K 8644, a dihydropyridine, stimulated calcitonin secretion in a dose dependent manner (10−7−10−5 M). This effect was completely inhibited by equimolar concentrations of the calcium channel blocker nifedipine and abolished in the absence of extracellular calcium. Similarly, nifedipine suppressed the stimulatory action of extracellular calcium. The effects of calcium and BAY K 8644 with and without nifedipine suggest that calcium influx via voltage dependent calcium channels plays an important role in calcitonin secretion. The primary cell culture of human medullary thyroid carcinoma is a good model for the study of stimulus secretion coupling.
    Type of Medium: Electronic Resource
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